Abstract
Toxoplasma gondii is known to have a complex life cycle and infect almost all kinds of warm-blooded animals around the world. The brain of the host could be persistently infected by cerebral cysts, and a variety of psychiatric disorders such as schizophrenia and suicide have been reported to be related with latent toxoplasmosis. The infected animals showed fear reduction and a tendency to be preyed upon. However, the mechanism of this “parasites manipulation” effects have not been elucidated. Here, we reviewed the recent infection prevalence of toxoplasmosis and the evidence of mental and behavioral disorders induced by T. gondii and discussed the related physiological basis including dopamine dysregulation and gamma-aminobutyric acid (GABA) pathway and the controversial opinion of the necessity for cerebral cysts existence. Based on the recent advances, we speculated that the neuroendocrine programs and neurotransmitter imbalance may play a key role in this process. Simultaneously, studies in the evaluation of the expression pattern of related genes, long noncoding RNAs (lncRNAs), and mRNAs of the host provides a new point for understanding the mechanism of neurotransmitter dysfunction induced by parasite manipulation. Therefore, we summarized the animal models, T. gondii strains, and behavioral tests used in the related epigenetic studies and the responsible epigenetic processes; pinpointed opportunities and challenges in future research including the causality evidence of human psychiatric disorders, the statistical analysis for rodent-infected host to be more vulnerable preyed upon; and identified responsible genes and drug targets through epigenetics.
Highlights
More than 110 years ago, Toxoplasma gondii was initially discovered in the tissues of a North African rodent Ctenodactylus gundi by Nicolle and Manceaux (1908) and was described in the tissues of a rabbit in 1908 by Splendore in Brazil (Chen et al, 2019)
Since the posttranslational modification (PTM) of histones plays a key role in epigenetic regulation and chromatin remodeling, similar PTM and gene expression changes in cyst-infected brain tissues would be another research direction to solve the mechanism of behavioral disorders induced by T. gondii
Up to now, advances of epigenetic regulation to explain the mechanism of T. gondii-induced mental and behavioral disorders showed an exciting achievement and reasonable orientation for discovering the mechanism, adequate epigenetic evidence associated with behavioral analysis is still lacking
Summary
More than 110 years ago, Toxoplasma gondii was initially discovered in the tissues of a North African rodent Ctenodactylus gundi by Nicolle and Manceaux (1908) and was described in the tissues of a rabbit in 1908 by Splendore in Brazil (Chen et al, 2019). More and more evidence has shown that latent toxoplasmosis may adversely affect individuals’ cognitive function and associate with mental disorders, violence, risk taking, personality changes, and cognitive impairments This evidence includes raised seropositivity of anti-toxoplasma antibodies among those with mental disorders, controlled behavioral analysis in humans, and experimental evidence in rodent models. A largescale case–control study including 81,912 blood donors by Burgdorf et al (2019) showed that T. gondii IgG seropositive rates were significantly associated with those of schizophrenia; they found a very weak association with traffic accident Another meta-analytic review involving a total of 2,553 patients and 1,703 controls confirmed the association, indicating that acute psychosis was significantly associated with acute Toxoplasma infection (IgM seropositive), and the association was stronger for patients with chronic schizophrenia. Two meta-analysis reports in this community showed that T. gondii infection increased the risk of traffic accidents, which might be related to “road rage” triggered
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